IgE bound to the surface of mast cells and/or basophils is responsible for the immediate hypersensitivity reaction. This response once established, persists for prolonged periods of time. We have shown that the mechanism is not due to internalization. Cross linking of the IgE by allergen (or other means) is normally necessary to elicit cell degranulation, which results in histamine release. We wished to determine if analogous, chemically induced cross-linking affects the fate of IgE compared to monomeric IgE. The possible effect of oligomerized IgE binding to the recently described IgG Fc of basophils was also being investigated. We found that IgE binds exclusively to its own (FcEpsilon) receptor and is internalized but not reexpressed upon cross-linking by "allergen" (ie, DNP-albumin + DNP-binding IgE). This is virtually unprecedented for known receptors.